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目的研究I-κBα在大鼠脑缺血再灌注损伤后作用的蛋白表达的时间和空间分布特点。方法应用Western Blot方法检测对照组及脑缺血2 h再灌注不同时程组(15 h、24 h、48 h)I-κBα蛋白表达水平,并用免疫组化技术研究I-κBα在脑缺血再灌注后作用的空间分布。结果Western Blot 研究发现I-κBα在对照组表达很低,于脑缺血2 h再灌注后15~24 h达到高峰,48 h始有所下降(P<0.01)。免疫组化研究发现:在半暗带的神经元、脑室壁和脉络丛及小血管内皮细胞均有I-κBα的阳性表达。结论由I-κBα介导的NF-κB 激活和抑制通路在局灶性脑缺血再灌注损伤的半暗带神经元的存活和血脑屏障中起重要作用。如能在一恰当的时间段内使用合成的I-κBα来抑制NF-κB的激活,可能是一潜在的保护脑组织的治疗途径。
Objective To study the temporal and spatial distribution of I-κBα protein after cerebral ischemia-reperfusion injury in rats. Methods Western Blot method was used to detect the expression of I-κBα protein in the control group and ischemia-reperfusion groups at different time points at 2 h (15 h, 24 h, 48 h). Immunocytochemistry was used to detect the expression of I-κB in cerebral ischemia The spatial distribution of the role after reperfusion. Results Western Blot showed that the expression of I-κBα was low in the control group, peaked at 15-24 hours after reperfusion at 2 hours and decreased at 48 hours (P <0.01). Immunohistochemical study found: In the penumbra neurons, ventricular wall and choroid plexus and small vascular endothelial cells have positive expression of I-κBα. Conclusion I-κBα-mediated NF-κB activation and inhibition pathways play an important role in the survival of the penumbra neurons and the blood-brain barrier after focal cerebral ischemia-reperfusion injury. Inhibition of NF-κB activation using synthetic I-κBα in an appropriate period of time may be a potential therapeutic approach to protecting brain tissue.